The mortality and morbidity due to group B streptococcal infections in neonates and other immunocompromised hosts remains exceedingly high in spite of the use of antibiotics and other support measures. We have demonstrated that patients who develop group B disease usually lack serum opsonins against their infecting strain and have defective phagocyte function. Moreover, there appear to be type and even strain specific differences in opsonic requirements for these organisms. The proposed studies were designed to determine specifically what antigel-antibody systems are responsible for opsonic activity with the 5 strains of this group and which are important in complement activation and animal protection. Furthermore, we will attempt to determine if maternal passive or active immunization can protect neonatal animals from group B infection. The role of administration of opsonic antibody and functional leukocytes in providing protection in this neonatal rat model will be determined. The mechanisms of group B streptococcal attachment to epithelial cells will also be investigated and surface factors important in this process identified. The role of antibody, complement and amniotic fluid factors in attachment will also be studied. Lastly, humoral and cellular immunity will be investigated in human neonatal and adult cases of group B disease. These studies will attempt to define the role of passive administration of antibody in altering morbidity and mortality due to this most fulminant of bacterial diseases.